Shewanella oneidensis MR-1 enhanced degradation of sulfamethoxazole (SMX) via a microbially driven Fenton reaction

Shewanella oneidednsis MR-1, a well-known Fe(III) respirating bacterium, can generate extracellular reactive oxygen species (ROS) in aerobic conditions. The ROS should be able to drive a microbial Fenton reaction to release hydroxyl free radicals able to attack the refractory emerging contaminants. In this study, an S. oneidensis MR 1 pure-culture was used to explore the performance and mechanism of microbially driven Fenton oxidation of the widely used antibiotic sulfamethoxazole (SMX). Over 16 days, SMX was repeatedly removed with anaerobic-aerobic cycling. HPLC-MS/MS analysis, combined with density functional theory (DFT) calculations, identified three SMX-degradation pathways that combined monooxygenase or N-acetyltransferase enzymatic co-metabolisms with extracellular hydroxyl attack. RNA-seq analysis provided transcriptomic evidence that the Mtr operon was involved in the extracellular ROS production. The EPS secretion system provided a defense response against hydroxyl damage. Moreover, cydA and cydB, which encode the cytochrome bd ubiquinol oxidase, were involved in O2 respiration and countering H2O2 stress during the microbially driven Fenton reaction. This study provides new insight into the degradation of SMX, a common sulfonamides antibiotic, based on the bio-Fenton reaction. In particular, the study provides the first transcriptomic evidence of the physiological mechanism for defending against extracellular ROS.